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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of brain infection with mouse hepatitis virus-JHM was studied in BALB/cByJ mice following intranasal inoculation, and found to be a consequence of direct viral spread along olfactory nerves into olfactory bulbs of the brain. Infection was followed sequentially from nose to brain, using microscopy, immunohistochemistry and virus quantification. Lesions, antigen and virus were observed in the olfactory bulb and anterior brain as early as 2 days and posterior brain by 4 days after inoculation. Viral antigen extended through nasal mucosa into submucosa, then coursed along the olfactory nerve perineurium and fibers, through the cribriform plate into the olfactory bulbs. On days 4 and 7, viral antigen was found in the antero-ventral brain, along ventral meninges, olfactory tracts and anterior ramifications of the lateral ventricles. Virus was cleared from nose by 10 days and anterior brain by 20 days, but persisted in posterior brain for 20 days after inoculation. Mice also developed disseminated infection, with viremia and hepatitis. Infection of brain did not correlate with presence of viremia. In contrast to intranasally inoculated mice, orally-inoculated mice did not develop encephalitis, despite evidence of disseminated infection.
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PMID:Olfactory neural pathway in mouse hepatitis virus nasoencephalitis. 284 76

Until 20 years ago the only chronic viral diseases known were those considered to be confined to the nervous system. As a result of recent advances in epidemiology, molecular biology and immunology, new viral diseases have been recognized and their clinical features and pathogenesis elucidated. Chronic disease may result from infection with the hepatitis B and D viruses and whatever agent or agents cause hepatitis non-A, non-B, the herpesviruses, Epstein-Barr virus, cytomegalovirus and human T-lymphotropic virus type III. These diseases have common features, including long-term or even lifetime asymptomatic carriage, viremia, with virus free in the plasma or attached to circulating mononuclear cells, presence of virus in body secretions, irreversible tissue injury in target organs and oncogenic potential. New information on these diseases is reviewed. Other chronic diseases for which the cause is currently unknown may eventually prove to be due to viral infection. In addition, vaccines may be developed for prophylaxis of some chronic viral diseases and associated malignant diseases.
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PMID:Chronic viral diseases. 302 3

We studied yellow fever virus infection in two species of monkey: Saimiri sciureus (squirrel monkeys) and Macaca mulatta (rhesus monkeys). Human gamma interferon was administered intravenously in five equal doses, one was given 24 hr before infection followed by four doses 24 hr apart. Interferon reduced the levels and duration of viremia and the severity of hepatitis in squirrel monkeys. Interferon prolonged survival time and delayed the appearance of viremia and hepatitis in infected rhesus monkeys, but it did not change overall mortality.
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PMID:Effect of human gamma interferon on yellow fever virus infection. 315 85

By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.
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PMID:Interferon treatment of chronic hepatitis B surface antigen (HBsAg) carriers. A description of the activation profiles of natural killer cells obtained with different schedules of administration in three subsets of carriers. 343 68

Homologous and heterologous haemagglutination-inhibition (HAI), complement-fixation (CF), immunodiffusion (ID) and mouse neutralization tests were performed with the Lunyo (LUN) and a Zimbabwean strain of Rift Valley fever (RVF) virus, the prototype and a South African strain of Arumowot (AMT) virus and prototype strains of Gordil (GOR), Saint-Floris (SAF) and Gabek Forest (GF) viruses, using immune mouse ascitic fluids prepared against these viruses. Reactions of identity occurred in all tests between LUN and the Zimbabwean strains of RVF and between the two strains of AMT virus. Otherwise, cross-reactions occurred between all the phleboviruses in HAI tests, while reactions in CF, ID and neutralization tests were monospecific for virus serotypes, except that weak cross-reaction occurred between GOR and SAF viruses in CF and ID tests. Four sheep infected subcutaneously with the Zimbabwean strain of RVF virus developed transient fever, viraemia, leucopaenia, relative thrombocytopaenia, haemoconcentration and raised serum enzyme levels, which indicated that the sheep had developed necrotic hepatitis. Disseminated focal necrotic hepatitis was confirmed in a sheep killed for examination on day 4 post-infection. The other three sheep recovered uneventfully after only mild depression and anorexia. Groups of three sheep infected with SAF, GOR, AMT and GF viruses had no demonstrable viraemia or other sign of infection or illness, except that the sheep infected with AMT developed mild fever lasting less than 24 h. Antibody responses were monitored at intervals over a period of 24 weeks in all sheep by homologous and heterologous HAI, CF and cell culture neutralization (CPENT) tests. Homologous antibody responses were marked in the RVF-infected sheep and their sera cross-reacted strongly in HAI tests with antigens of the other viruses. The sera of the RVF-infected sheep cross-reacted less markedly in CF and CPENT tests. Homologous antibody responses were poor in all the sheep infected with phleboviruses other than RVF, and the cross-reactivity of their sera for RVF antigen or virus was negligible. All sheep were challenged with RVF virus 48 weeks after their initial infection. The sheep which had originally been infected with RVF virus were immune and developed neither fever nor viraemia. All other sheep developed fever, viraemia and antibodies to RVF virus. It was concluded that the African phleboviruses, other than RVF, are unlikely to cause disease in livestock or to induce antibodies which could cause confusion in the diagnosis of RVF.
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PMID:Comparative pathogenicity and antigenic cross-reactivity of Rift Valley fever and other African phleboviruses in sheep. 353 19

To understand the relationship among the time of infection, infection patterns, and liver diseases, experimental transmission of duck hepatitis B virus (DHBV) utilizing 165 Japanese white domestic ducklings was performed. Twenty to 25 ducklings were each inoculated with DHBV-positive serum intravenously at day one, 3, 5, 7, 10, and 14 posthatch and were sacrificed during the 1st, 2nd, 3rd, and 4th (and 24th in those inoculated on day one and day 3 posthatch) week after inoculation to obtain sera and the liver. The sera served for the measurement of DHBV DNA by spot hybridization test and DNA polymerase activity, and the liver was subjected to morphological examination including immunostaining for DHBV. The ducklings inoculated with DHBV on 1 day and 3 days posthatch always revealed persistent viremia, whereas those on and after 5 days posthatch showed persistent or transient viremia. The hepatitis activity in the liver was seen in ducklings inoculated with DHBV on and after 3 days posthatch and was very weak consistent with the diagnosis of mild acute hepatitis of humans. The serum transaminase activity was not significantly elevated at the time of occurrence of histological hepatitis activity. Since host immune mechanism establish at 3 to 5 days posthatch in birds, the host immune response seemed to determine whether DHBV infection was persistent or transient and the occurrence of hepatitis activity as seen in human hepatitis B virus (HBV) infection.
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PMID:A sequential study of viral DNA in serum in experimental transmission of duck hepatitis B virus. 358 87

We investigated experimental transmission of duck hepatitis B virus to its original host, the domestic Pekin duck, and to three other avian species. Intramuscular injection of a standard inoculum of duck hepatitis B virus into 2- to 5-day-old Pekin ducklings hatched from a duck hepatitis B virus-free flock resulted in viremia in 100% of 107 animals, indicating that duck hepatitis B virus infection of young progeny of a defined duck hepatitis B virus-free flock occurs reproducibly. When the same inoculum was injected into chicks and Muscovy ducklings of the same age, no evidence of viral infection was detectable. In contrast, hatchlings of two domestic breeds of geese were readily infected by duck hepatitis B virus, developing viremia at a slower rate than Pekin ducklings, but a higher average titer of viremia 4 weeks or more after injection. Neither the pattern of restriction enzyme sites in the viral DNA nor the susceptibility of ducklings to the virus were detectably altered after passage in geese. As in duck hepatitis B virus-infected young ducklings, most of the experimentally infected goslings appeared to be persistently infected and those eventually laying eggs transmitted virus to the progeny. While ducklings exhibited a fairly uniform inflammatory response to the virus, duck hepatitis B virus inoculation of the goslings resulted in both inflammation and an altered hepatocellular morphology not seen in uninjected controls. The host range of duck hepatitis B virus appears to be limited to the primary host and a close taxonomic relative, similar to other members of the hepadnavirus family, hepatitis B virus and ground squirrel hepatitis virus.
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PMID:Experimental transmission of duck hepatitis B virus to Pekin ducks and to domestic geese. 361 50

Immunization of monkeys with yellow fever virus-specified nonstructural protein NS1 resulted in protection against fatal hepatitis as well as marked reduction in the magnitude of viremia after subcutaneous challenge with yellow fever virus. The results may be relevant to the design of possible subunit or recombinant flavivirus vaccines.
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PMID:Protection against yellow fever in monkeys by immunization with yellow fever virus nonstructural protein NS1. 378 16

The periods of persisting immunoglobulin M class antibodies to hepatitis B core antigen in 28 patients with acute hepatitis B infections and in 134 patients with chronic hepatitis B infections were studied by using an enzyme-linked immunosorbent assay and an indirect immunofluorescence technique. We showed that the clearance of antibodies to hepatitis B core antigen is independent of the degree of viremia in both forms of hepatitis.
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PMID:Evidence for limited humoral immunoglobulin M antibody response to hepatitis B core antigen during acute and chronic hepatitis B virus infections. 389 72

The risk of hepatitis B infections has been reduced by screening of blood donors for hepatitis B surface antigen (HBsAg). However, recipients remain at significant risk of developing post-transfusion hepatitis. Studies have shown that non-A, non-B hepatitis virus(es) are responsible for the majority of post-transfusion hepatitis infections. In spite of many efforts, these non-A, non-B hepatitis viruses have not yet been identified. Epidemiological studies, however, suggest that non-A, non-B hepatitis shares many features with hepatitis B. Recently, Wands et al [1982] showed, in chimpanzees infected with non-A, non-B hepatitis agents, the presence of antigenemia or viremia by radioimmunoassay with monoclonal antibodies directed toward distinct determinants of HBsAg and by molecular hybridization analysis. They suggested that non-A, non-B hepatitis agents may be related, but distinct variant(s) of hepatitis B virus (HBV). In this study, five chimpanzees were inoculated with three different agents that have been shown to transmit non-A, non-B hepatitis. The following inocula were used (I) a factor VIII preparation kindly provided by D.W. Bradley, (II) acute phase serum from a chimpanzee infected with the F strain kindly provided by A.J. Zuckerman, and (III) a DS-antigen serum previously shown by us to transmit non-A, non-B hepatitis [Duermeyer et al, 1983]. All chimpanzees developed a rise in transaminase levels between 8 and 10 weeks after inoculation. None of the chimpanzees was positive for any markers of HBV infection. No evidence was obtained of infection with hepatitis A, cytomegalovirus, or Epstein-Barr virus. One chimpanzee developed chronic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of detectable hepatitis B virus DNA in sera and liver of chimpanzees with non-A, non-B hepatitis. 392 Mar 54


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